ArticleThe Journal of cell biology2012
JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
66 citing papers in PubMed, 96 citations in OpenAlex.
- Shared and Tissue-Specific Expression Signatures between Bone Marrow from Primary Myelofibrosis and Essential Thrombocythemia.Experimental hematology · 2019Trial
- Substrate stiffness dictates unique paths towards proliferative arrest in WI-38 cells.GeroScience · 2026Article
- JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.Biology direct · 2026Article
- Review
- SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026Review
- Repurposing Artesunate to Combat Progression and Metastasis via Targeting Circulating Tumor Cells.Oncology research · 2026Article
- Massively parallel analysis of genotype-dependent enhancer activity among atopic dermatitis genetic risk variants.The Journal of allergy and clinical immunology · 2025Article
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- Exploring the Cellular and Molecular Landscape of Idiopathic Pulmonary Fibrosis: Integrative Multi-Omics and Single-Cell Analysis.Biomedicines · 2025Article
- ELF3 regulates epithelial-mesenchymal transition through TPM1 and promotes the development of endometrial cancer.Cytotechnology · 2025Article
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genome-wide DNA methylation analysis of Astragalus on the intervention of ID2 promoter via PI3K/Akt signaling pathway in peritoneal fibrosis.Scientific reports · 2025Article
- Transcription factor JUNB is required for transformation of EpCAM-positive hepatocellular carcinoma (HCC) cells into CD90-positive HCC cells in vitro.Cell death & disease · 2025Article
- Histone H3E50K remodels chromatin to confer oncogenic activity and support an EMT phenotype.NAR cancer · 2025Article
- Transcriptional regulators ensuring specific gene expression and decision-making at high TGFβ doses.Life science alliance · 2025Article
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- ADAMTS12 promotes fibrosis by restructuring extracellular matrix to enable activation of injury-responsive fibroblasts.The Journal of clinical investigation · 2024Article
- Relevance Analysis of TPM2 and Clinicopathological Characteristics in Breast Cancer.International journal of general medicine · 2024Article
- Machine Learning and Single-Cell Analysis Identify Molecular Features of IPF-Associated Fibroblast Subtypes and Their Implications on IPF Prognosis.International journal of molecular sciences · 2023Article
- Progenitor-derived glia are required for spinal cord regeneration in zebrafish.Development (Cambridge, England) · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The process of epithelial-mesenchymal transition (EMT) in response to transforming growth factor-β (TGF-β) contributes to tissue fibrosis, wound healing, and cancer via a mechanism that is not fully understood. This study identifies a critical role of JunB in the EMT and profibrotic responses to TGF-β. Depletion of JunB by small interfering ribonucleic acid abrogates TGF-β-induced disruption of cell-cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins. JunB contributes to Smad-mediated repression of inhibitor of differentiation 2 through interaction with transcription repressor activating transcription factor 3. Importantly, JunB mediates the TGF-β induction of profibrotic response factors, fibronectin, fibulin-2, tropomyosin (Tpm1), and integrin-β3, which play critical roles in matrix deposition, cell-matrix adhesion, and actin stress fibers. In summary, JunB provides important input in setting the transcriptional program of the EMT and profibrotic responses to TGF-β. Thus, JunB represents an important target in diseases associated with EMT, including cancer and fibrosis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.